Emotional Processing and the Brain
Given the differences between cognitive and emotional aging, a number of questions have served to guide contemporary research in the area of emotional processing. Such questions include: what declines, what is preserved, and what improves? In addition, it is important to identify the conditions under which we observe decline, preservation, and improvement. The neuroscience approach takes this a step further by identifying the specific biological mechanism reflected in the structure and activation patterns of the brain associated with, for example, preserved emotional processing.
As we saw in the cognitive neuroscience section, neuroimaging allows us to identify brain regions of activation that underlie successful information processing, for example, activation of the prefrontal cortex (PFC) during encoding relates to better memory. Much behavioral work indicates that if information has emotional significance, we will more likely remember it than information that is more neutral in nature. A number of researchers have been interested in uncovering the neural circuitry that is most responsible for this enhanced memory for emotional information (e. g., Kensinger & Corkin, 2004).
Kensinger and colleagues (Kensinger, 2006; Kensinger & Corkin, 2004) propose two distinct cognitive and neural processes that contribute to emotional memory enhancement. Processing of negative high-arousal information for memory is relatively automatic in nature and is linked to activation of the amygdala as it interacts with the hippocampus to support memory performance. For memory processing of negative low-arousal stimuli, more activation of the prefrontal cortex – hippocampus network is necessary. This area is associated with controlled self-generated encoding processes (Kensinger & Corkin, 2004). Kensinger
(2006) argues that emotional enhancement in memory for detail is a result of more engagement in emotion-specific processes that are linked to these distinct neural processes. Thus, when one accurately remembers negative high-arousal items, this corresponds to increased activation of the amygdala and orbitofrontal cortex. Other studies support this in that if the amygdala is damaged, individuals do not attend to arousing stimuli. How do structural and functional changes in the brain affect these processes?